Effects Of Acute Volume Expansion Research Articles

Comparative effects of acute volume expansion and short-term training on thermal and cardiovascular responses to prolonged exercise

Comparative effects of acute volume expansion and short-term training on thermal and cardiovascular responses to prolonged exercise

Effect of acute volume expansion associated with salt load on the profile of plasma angiotensins in rats

We measured the changes produced in renin and the peptide components of the circulating renin-angiotensin system by acute volume expansion alone or associated with salt load in rats. With both maneuvers, there was a decrease of plasma renin activity (PRA) and plasma angiotensin (Ang) concentrations, but the changes were more pronounced in the salt-load group. In contrasting to Ang I and Ang II, plasma Ang-(1–7) concentration decreased significantly only within 60 min of 5.0% NaCl infusion (19.5 ± 2.9 vs 30.5 ± 1.9 pg/ml in the control group). As expected, plasma vasopressin increased markedly in the animals submitted to acute salt load (144.0 ± 42.0 vs 5.0 ± 0.2 pg/ml in the control group). The dissociation between the changes in plasma Ang-(1–7) and that of other plasma angiotensins is consistent with our previous studies using chronic salt load, and suggests that during acute volume expansion associated with salt load Ang I is preferentially converted to Ang-(1–7). In contrast to vasopressin, however, plasma Ang-(1–7) concentration increased only after chronic salt load, suggesting that this angiotensin may be more involved with long-term mechanisms of control of hydromineral balance.

Comparative effects of acute volume expansion and short-term training on thermal and cardiovascular responses to prolonged exercise

To investigate the hypothesis that increases in plasma volume (PV) are crucial to the cardiovascular and thermal adaptations resulting from training, eight moderately active males (Vo2max = 4.10 +/- 0.32 L/min; mean +/- SE) performed prolonged cycle exercise at 60% Vo2max during a control test (CON) and following infusion (10 mL/kg) of a 6% dextran solution (DEX). These responses were also compared with short-term training (TR) involving 3 days of cycling for 90-120 min at moderate intensity (60% Vo2max). During DEX, exercise cardiac output (Q) and stroke volume (SV) were persistently higher (p < 0.05) than CON, while heart rate (HR) was unchanged. In comparison, TR resulted in a lower (p < 0.05) HR at constant Q. In contrast with TR, in which the exercise response was unchanged from CON, the DEX condition produced a lower total peripheral resistance. Rectal temperature (Tre) was lowered (p < 0.05) both by DEX and TR, but the conditions differed in the time at which the reduction occurred. For DEX, the lower Tre was manifested early and persisted throughout exercise, whereas for TR the Tre was only lower later in exercise. Forearm blood flow, mean skin temperature, and sweat rate were not affected by DEX or TR. It is concluded that acute PV expansion does not affect the time-dependent response in cardiovascular function or thermoregulation during prolonged exercise in ambient conditions. The primary effects appear to be manifested during rest or soon after the onset of exercise.

Influence of Extracellular Volume Expansion on Circulating PTH1-84 in Subjects With Mild Essential Hypertension

The effect of acute volume expansion by saline (1 L/40 min) on serum parathyroid hormone (PTH) concentration was studied in 28 subjects with mild essential hypertension. At the zenith volume expansion there was a significant increase in systolic pressure (7 +/- 2 mm Hg, P < .01) while diastolic pressure and heart rate showed minor (NS) variations. The rise in systolic pressure was accompanied by a significant (P = .02) decrease in plasma ionized calcium (from 1.12 +/- 0.03 to 1.08 +/- 0.03 mmol/L) and by a marked PTH increase (from 36 +/- 3 to 60 +/- 4 pg/mL, P < .01). The arterial pressure variations were independent of changes in serum PTH. In a second experiment (n = 11), aimed at preventing the changes in calcium concentration brought about by hemodilution, we infused the same volume of saline with the addition of 1.25 mmol of elemental calcium. In this study PTH showed a small, nonsignificant, decrease while systolic pressure changes were similar to those of the first study (ie, an isolated 9 +/- 4 mm Hg increase in systolic pressure). In a third experiment (n = 7), aimed at studying the effect of raised plasma PTH concentration in isocalcemic conditions, PTH1-38 was continuously infused (1 ng/kg/min) during the volume expansion phase performed with the same solution as used in the second experiment. The hemodynamic changes were again identical to those of the other studies (an isolated 9 +/- 3 mm Hg increase in systolic pressure).(ABSTRACT TRUNCATED AT 250 WORDS)

The effect of acute volume expansion and vasodilatation with verapamil on uterine and umbilical artery Doppler indices in severe preeclampsia

Preeclampsia is associated with increased peripheral, uterine, and umbilical artery resistance. Acute blood pressure reduction may result in shunting of blood and sudden fetal distress. We therefore investigated the effects of volume expansion and verapamil therapy on uteroplacental and umbilical resistance during treatment of preeclampsia. Five severe preeclamptics underwent volume expansion and subsequent vasodilatation with an infusion of verapamil. Invasive hemodynamic monitoring and Doppler ultrasonography were used to study changes in maternal, uterine, and umbilical hemodynamics. Volume expansion and subsequent verapamil therapy was associated with significant changes in maternal hemodynamics without significant change in uteroplacental or umbilical resistance. Uterine artery waveform changes were noted, with disappearance of notching in some cases. Volume expansion and verapamil therapy effectively reduces maternal blood pressure in preeclampsia, without adversely affecting uteroplacental or umbilical artery resistance. Uterine artery waveform changes may be associated with improved fetal outcome.

Acute volume expansion in normal pregnancy and preeclampsia. Effects on plasma atrial natriuretic peptide (ANP) and cyclic guanosine monophosphate (cGMP) concentrations and feto-maternal circulation.

To compare normal pregnancy with pregnancy-induced hypertension (PIH)/preeclampsia with respect to the effects of acute volume expansion on plasma atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP) and fetal-maternal circulation. Observational study. University hospital. Fifteen women with PIH/preeclampsia and 15 healthy pregnant controls. Before and after 30 minutes' infusion of a crystalloid solution (15 ml/kg), maternal venous blood was sampled for ANP and cGMP analysis and echocardiographic and Doppler investigations were performed. Basal median (range) ANP and cGMP levels were significantly higher in the PIH/preeclampsia group compared to the controls: 6.5 (3.8-30.4) compared to 3.9 (2.0-6.7) pmol/l, p < 0.01 and 5.8 (2.4-11.6) compared to 4.0 (2.3-10.8) nmol/l, p < 0.05. The response to volume load was enhanced: 4.6 (-4.5-21.8) compared to 0.7 (-4.1-8.8), p < 0.05 and 2.9 (0.1-10.9) compared to 1.2 (-5.0-6.0), p < 0.05, respectively. Systemic vascular resistance was initially higher in the patient group, 22.3 (14.1-36.7) compared to 15.6 (10.0-25.5) peripheral resistance units, p < 0.01 but the response to volume load was similar in both groups (12-13% decrease). The pulsatility index of the uterine artery, 0.85 (0.46-1.38) compared to 0.72 (0.49-1.26) and umbilical artery 0.89 (0.66-1.57) compared to 0.97 (0.74-1.31) did not differ between the groups. Volume expansion did not affect any of these variables. The pulsatility index of the uterine artery remained unaffected in both preeclamptic patients and healthy controls despite an increase of ANP and cGMP concentration and a systemic vasodilatation during acute volume expansion. This finding may indicate the absence of a vasodilation of the uteroplacental vascular bed.

Acute volume expansion enhances baroreceptor discharge in dogs

By recording single-unit discharge from the carotid sinus nerve of normal dogs in the control and in the volume-expanded state, both with the sinus open to the circulation and with it isolated, the effects of acute volume expansion on baroreceptor discharge sensitivity were investigated. The carotid sinus was vascularly isolated except for the common carotid and external carotid arteries. Inflation of hydraulic occluders on these vessels completely isolated the sinus from the systemic circulation. Flow and diameter changes of the carotid sinus were measured. Plasma volume was expanded with isotonic, isoncotic dextran in normal saline until the left ventricular end-diastolic pressure reached a value of 20-25 mmHg. In the group with the sinus open to the circulation, volume expansion did not depress baroreceptor discharge sensitivity; in fact, it augmented baroreceptor activity (peak discharge = 39.2 +/- 1.6 vs. 49.9 +/- 3.3 spikes/s, P less than 0.05). There was no such effect in the group with the sinus isolated from the circulation during volume expansion. In the group with the sinus open to the circulation, volume expansion significantly increased flow through the common carotid artery and shifted the carotid sinus pressure-diameter curves upward without a change in compliance. These data suggest that acute volume expansion augments baroreceptor discharge, and this phenomenon may be mediated either by some circulating substance(s) or by an increase in flow through the carotid sinus during volume expansion.

Acute volume expansion in normal pregnancy and preeclampsia

Objective. To compare normal pregnancy with pregnancy-induced hypertension (PIH)/preec-lampsia with respect to the effects of acute volume expansion on plasma atrial natriuretic peptide (ANP), cyclic guanosine monophosphate (cGMP) and fetal-maternal circulation. Design. Observational study.Setting. University hospital.Subjects. Fifteen women with PIH/ preeclampsia and 15 healthy pregnant controls. Interventions. Before and after 30 minutes' infusion of a crystalloid solution (15 ml/kg), maternal venous blood was sampled for ANP and cGMP analysis and echocardiography and Doppler investigations were performed.Results. Basal median (range) ANP and cGMP levels were significantly higher in the PIH/ preeclampsia group compared to the controls: 6.5 (3.8-30.4) compared to 3.9 (2.0-6.7) pmol/1, p≤0.01 and 5.8 (2.4-11.6) compared to 4.0 (2.3-10.8) nmol/1, p≤0.05. The response to volume load was enhanced: 4.6 (-4.5-21.8) compared to 0.7 (-4.1-8.8), p≤0.05 and 2.9 (0.1-10.9) compared to 1.2 (- 5.0-6.0), p≤0.05, respe...

Quantitative Hemodynamic Effects of Acute Volume Expansion in Severe Preeclampsia

The role of acute volume expansion in severe preeclampsia remains controversial, with advocates claiming an improvement in maternal hemodynamics and maternal-fetal status whereas opponents fearing severe hypertensive responses and the risk of pulmonary edema.

Role of kidney dopamine in the natriuretic response to volume expansion in rats.

It has been postulated that endogenously produced dopamine (DA) may play a role in the regulation of renal sodium excretion. In the present study, experiments were designed to test the hypothesis that acute volume expansion with isotonic sodium chloride stimulates the production of DA within the kidney, which in turn acts on specific DA1 receptors to promote sodium excretion. In pentobarbital-anesthetized rats, acute volume expansion over a period of 1 hour evoked a pronounced increase in urine output and urinary sodium excretion. These diuretic and natriuretic effects were not accompanied by any significant changes in blood pressure or heart rate. However, there was a significant elevation in central venous pressure and a transient rise in glomerular filtration rate. The natriuretic and diuretic response was accompanied by a significant increase in urinary DA excretion, and this effect was clearly dissociated from the rise in glomerular filtration rate. In a separate group of rats, the effects of acute volume expansion were studied in the presence of selective DA1 receptor antagonist SCH-23390 (50 micrograms/kg i.v. bolus; 10 micrograms/kg/min). During DA1 receptor blockade, there was a marked attenuation in the diuretic and natriuretic response throughout the period of volume expansion, when compared with that in the control group. The changes in central venous pressure and glomerular filtration rate were identical in the two groups. In another group of rats, the renal effects of exogenously administered DA were studied. DA (0.5 micrograms/kg/min) produced significant increases in urine output and urinary sodium excretion, without causing any alterations in blood pressure or glomerular filtration rate, suggesting a tubular site of action.(ABSTRACT TRUNCATED AT 250 WORDS)

Glomerular filtration effects of acute volume expansion: Importance of chloride

The present studies were done to determine the effect on GFR of acute volume expansion (AVE) using solutions of various sodium salts and to explore if degree of tubuloglomerular feedback (TGF) activation plays a role in any GFR differences. Free-flow micropuncture and inulin clearance studies were combined to investigate anesthetized Munich-Wistar rats expanded to 10% body weight with isotonic solutions of NaCl, Ringers bicarbonate (RB), NaHCO3, Na acetate (NaAc) and Na2SO4 as well as euvolemic controls. In the clearance studies, AVE yielded per gram kidney weight GFR's greater than control (1009 +/- 51 microliter/min) in the NaCl and RB (chloride expanded) groups (1397 +/- 89 and 1389 +/- 64) microliter/min, respectively, P less than 0.05 vs. control) but not in the NaHCO3, NaAc, and Na2SO4 (non-chloride expanded) groups. Proximal minus distal single nephron GFR determinations (P-D), an estimate of the degree of TGF, were less than control 13.2 +/- 2.1 nl/min) in the NaCl and RB groups (4.1 +/- 0.7 and 5.3 +/- 1.9 nl/min, respectively, P less than 0.05 vs. control) but were not significantly different from control in any of the non-chloride expanded groups. Early distal (ED) fluid flow correlated positively with P-D in all groups. ED chloride concentration but not TCO2 nor osmolality correlated with P-D for all groups. The correlation was negative for control and chloride expanded groups and positive for non-chloride expanded groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial natriuretic factor in sodium-sensitive and sodium-resistant Dahl rats.

We tested the hypothesis that atrial natriuretic factor (ANF) may play a role in the development of hypertension in salt-sensitive Dahl (S) rats as compared to normotensive salt-resistant Dahl (R) rats. We measured immunoreactive ANF in plasma and atria of the inbred (JR) strain of Dahl S and R rats receiving 0.9 or 8% NaCl diets for up to 8 weeks. We also tested the effect of acute volume expansion on plasma and atrial ANF values in rats receiving the 0.9% salt diet. In addition, we examined the effects of exogenous ANF in the form of atriopeptin III given as intravenous bolus infusion at both levels of salt intake. We found no difference in plasma and atrial values between S and R rats irrespective of salt intake. The S and R rats showed a similar, five- to sevenfold increase of plasma ANF in response to acute saline expansion. Finally, we were unable to demonstrate differences between S and R rats in response to atriopeptin III with respect to transient decreases in blood pressure, and pronounced increases in glomerular filtration rate (GFR), renal blood flow or natriuresis. These results do not reveal appreciable changes in the ANF system of Dahl S rats either before or after onset of hypertension when compared to normotensive R rats. Therefore, our findings do not support the notion that ANF is important in the development or maintenance of chronic salt-induced hypertension in S rats.

Dissociation between changes in renal nerve activity and renal vascular resistance in conscious dogs.

The effects of acute volume expansion and hemorrhage on renal nerve activity and renal vascular resistance were examined in chronically instrumented conscious dogs. In six conscious dogs, when the blood volume was expanded by 18 ml/kg, the mean arterial pressure increased by 14 +/- 3 mmHg, mean left atrial pressure increased by 5.3 +/- 0.7 mmHg, and renal nerve activity decreased by 87 +/- 3%, while the renal blood flow was not altered significantly and renal vasoconstriction occurred, i.e., the calculated renal vascular resistance increased by 12 +/- 4% from 0.49 +/- 0.05 mmHg/ml/min. Volume depletion, induced by 20 ml/kg hemorrhage, did not alter the mean arterial pressure (-4 +/- 6 mmHg), while it decreased the mean left atrial pressure by 4.0 +/- 0.7 mmHg and increased the renal nerve activity by 200 +/- 67%. However, the renal blood flow was well maintained at the pre-hemorrhagic control level and renal vasoconstriction did not occur. Thus, in conscious dogs, acute volume changes altered the renal nerve activity dramatically, but these changes in renal nerve activity did not exert any significant effects on renal vascular resistance.

Plasma Levels of Atrial Natriuretic Peptides in Conscious Adult Spontaneously Hypertensive Rats

The effects of acute volume expansion and acute salt loading on the plasma levels of immunoreactive atrial natriuretic peptides (ir-ANP's) were investigated in conscious adult (16 weeks) Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR). Basal plasma concentrations of ir-ANP's were similar (108 +/- 9 pg/ml and 105 +/- 8 pg/ml, respectively) in hypertensive and normotensive rats. In both strains mean arterial pressure, heart rate and plasma catecholamines were unaltered by acute volume expansion but significantly elevated by acute salt loading. However, both acute volume expansion and acute salt loading increased plasma concentrations of ir-ANP's similarily in SHR and WKY rats, independent of blood pressure or plasma catecholamine levels. Our findings show that chronic hypertension in SHR does not result in changes in basal or VOL- and SAL-stimulated levels of circulating ir-ANP's.

Effects of volume expansion on renal nerve activity, renal blood flow, and sodium and water excretion in conscious dogs

Effects of acute volume expansion with isotonic isoncotic 3% dextran in saline were examined on renal nerve activity (RNA), renal blood flow, vascular resistance, and sodium and water excretion in conscious dogs. In intact dogs, acute volume expansion increased mean arterial pressure 15 +/- 3 mmHg, left atrial pressure 5.5 +/- 0.6 mmHg, and decreased RNA 88 +/- 2%, whereas renal blood flow did not change and renal vascular resistance increased slightly. When renal perfusion pressure was maintained at control levels, volume expansion decreased RNA 87 +/- 2% and renal vascular resistance 15 +/- 4%. During the 80-min period after volume expansion, urine flow rate increased 0.66 +/- 0.13 ml/min and sodium excretion rose 3.89 +/- 0.54 mueq X min-1 X kg-1, whereas RNA remained depressed. Arterial baroreceptor denervation (ABD) did not diminish responses of RNA, renal blood flow, renal vascular resistance, or sodium and water excretion to volume expansion. After ABD plus bilateral cervical vagotomy, volume expansion did not decrease RNA, and diuretic and natriuretic responses were significantly attenuated (P less than 0.025). However, responses of renal blood flow to volume expansion were not altered significantly. In conscious dogs with renal denervation, responses of renal blood flow to volume expansion were not impaired, whereas diuretic and natriuretic responses were attenuated (P less than 0.025). Thus, in intact conscious dogs, vagally mediated reflex decreases in RNA induced by acute volume expansion exerted a significant effect on sodium and water excretion but little control of renal blood flow and renal vascular resistance.

Effects of acute blood volume expansion on vascular resistance and reactivity in anaesthetized dogs.

1. The effects of acute volume expansion on vascular resistance and reactivity to noradrenaline and angiotensin II are reported in this study. The estimated circulating blood volume of pentobartibal-anaesthetized dogs was expanded by about 35% with equilibrated donor blood. The animals were bilaterally nephrectomized to sustain expanded volume. 2. Functional changes in vascular smooth muscle were determined in the flow controlled, vascularly isolated, denervated, perfused hind limb preparation in the same animal. 3. Systemic volume expansion per se had no immediate influence on vascular resistance. However, resistance in the hind limb, as determined by the shift of the pressure-flow curves, progressively increased 60 and 120 min after volume expansion. The changes noted after 120 min were significantly greater than those observed after 60 min. 4. The changes in vascular resistance were accompanied by potentiation of the vascular responses to noradrenaline but not to angiotensin II. Significant shifts which occurred in the noradrenaline dose-response curves were similar to those of the resistance curves. 5. in closely simulated control experiments in dogs whose kidneys were intact or had been removed, and whose blood had or had not been equilibrated with donor blood, the above-mentioned vascular changes were not observed in the absence of volume expansion. 6. It is suggested that the functional changes observed in the hind limb vasculature after volume expansion are related to the presence of a circulating substance. From the data obtained from the experimental model used in this study, it can be concluded that such a substance is not released from the kidney.

Effect of volume expansion and plasma chloride on function of the loop segment.

To determine the effect of acute volume expansion and changes in plasma chloride on fluid and chloride uptake in superficial loop segments of rats, this segment was microperfused in vivo at 22 nl/min with a fluid containing Na 145, Cl and 36Cl 130, and HCO3 15 meq/liter during hydropenia and after acute volume expansion with 0.15 M NaCl, 0.15 M NaHCO3, or an isotonic bicarbonate Ringer (Cl 106 meq/liter) solution. Fractional fluid, chloride, and 36Cl reabsorption and early distal chloride concentration did not change during maintained hydropenia (time control) or during volume expansion with NaCl (plasma chloride 120 meq/liter) or bicarbonate Ringer solution (plasma chloride 104 meq/liter). Absolute and fractional reabsorption of chloride and 36Cl increased, without change in fluid reabsorption, and early distal chloride diminished after infusion of NaHCO3 (plasma chloride 90 meq/liter). It is concluded that acute volume expansion, per se, has no effect on either net fluid or net chloride absorption in the superficial loop segment at the load studied. Hypochloremia is associated with increased net reabsorption of chloride and an increased unidirectional efflux of chloride from the loop segment during acute volume expansion, most likely due to a gradient effect on the thick ascending limb of the loop of Henle.

Sodium permeability of rat proximal tubules: Effect of acute volume expansion and homologous harvested proximal tubular fluid

Sodium permeability of rat proximal tubules: Effect of acute volume expansion and homologous harvested proximal tubular fluid

Effect of volume expansion on pressor response to angiotensin II in pregnant ewes.

Vascular refractoriness to infused angiotensin II (AII) characterizes normal human and ovine pregnancy. To ascertain whether the refractoriness in the gravid ewe is mediated by either endogenous plasma concentrations of renin and AII or vasomotor reflexes, effects of acute volume expansion (VE) on the pressor response to AII were studied in chronically instrumented nonpregnant and near-term pregnant sheep. Dose-response curves describing the pressor response (delta BP) were determined before and after infusions of 1.0 1 of isotonic saline (NS) or 0.5 1 of 10% dextran (D). In nonpregnant sheep, hematocrit (Hct) and plasma renin activity (PRA) fell in all animals after NS (n = 7) and D (n = 6) (P less than 0.005). After VE with NS and D, delta BP increased at each dose of AII (P less than 0.05). The pressor response to AII in pregnant sheep was not altered by NS although decreases in Hct and PRA were comparable to those in nonpregnant sheep. Baroreceptor responses were not altered. Vascular refractoriness to infused AII in pregnant sheep is not due primarily to changes in plasma concentrations of renin-AII but more likely to another factor, vessel wall refractoriness. In this respect, the ewe is similar to the human.

Glomerular filtration dynamics in the dog during elevated plasma colloid osmotic pressure

To determine if the glomerular filtration coefficient (Kf) of the dog is influenced by changes in plasma colloid osmotic pressure (COP), we conducted micropuncture experiments in dogs given concentrated albumin solutions. In one group (N = 9), filtration dynamics were evaluated following infusion of 450 to 600 ml of a 25% bovine albumin solution. To minimize the effects of acute volume expansion, we also achieved high COP levels in another group (N = 7) by albumin loading on the day prior to the experiment. In all experiments, renal arterial pressure was reduced to approximately 90 mm Hg to minimize potential errors that might lead to overestimation of single nephron filtration rate (SNGFR) and glomerular pressure (GP). In the acutely expanded dogs, COP increased to 23.0 +/- (SEM) 0.9 mm Hg, SNGFR was 59 +/- 6 nl/min, estimated GP was 61.0 +/- 2.0 mm Hg, proximal tubule pressure (PTP) was 23.0 +/- 1.6 mm Hg, and superficial filtration fraction (SFF) was 0.13 +/- 0.02. A similarly reduced whole kidney filtration fraction was also observed, due almost entirely to a marked increase in renal blood flow. When compared to noninfused control dogs (N = 13), Kf was significantly higher in the dogs with elevated COP, being 5.3 +/- 0.6 nl/min/mm Hg as compared to 3.4 +/- 0.3 nl/min/mm Hg. Average effective filtration pressure (EFP) was 12 +/- 1mm Hg, and EFP at the efferent end of the glomerular capillaries was 8.9 +/- 1.2 mm Hg. In the group infused on the prior day, COP was 20.0 +/- 0.8 mm Hg, SFF was 0.26 +/- 0.01, SNGFR was 70 +/-8 nl/min, GP was 59 +/- 2 mm Hg, and PTP was 19.0 +/- 1.5 mm Hg. Average EFP was 15 +/- 1 mm Hg, and EFP at the efferent end of the capillaries was 7.5 +/- 0.7 mm Hg. kf was 4.85 +/- 0.66 nl/min/mm Hg, a value significantly higher than that obtained in control dogs having a COP of 15.0 +/- 0.6 mm Hg. Furthermore, one group of control dogs (N = 4), expanded with an isooncotic albumin solution, did not exhibit significant changes in Kf even though the degree of plasma volume expansion was similar to the group expanded with concentrated albumin solution. These experiments are consistent with previous findings obtained in the rat that Kf is influenced by the COP, although the changes in Kf appear to be less than they are in the rat. The data indicate that even under these conditions of elevated COP, the filtration process in the dog is characterized by positive filtration pressures throughout the length of the glomerular capillaries.